title: Perforin-mediated cytotoxicity in non-ST elevation myocardial infarction.
abstract: The aim of this investigation was to examine the role of perforin (P)-mediated cytotoxicity in the dynamics of tissue damage in patients with non-ST-segment elevation myocardial infarction (NSTEMI) treated with anti-ischaemic drugs. We enrolled 48 patients with NSTEMI in this study [age, 71.5 years; 61.5/76 (median, 25th/75th percentiles)]. The percentage of total peripheral blood P(+) lymphocytes was elevated owing to the increased frequency of P(+) cells within natural killer (NK) subsets, T and NKT cells in patients on day 1 after NSTEMI when compared with healthy controls. Positive correlations were found between cardiac troponin I plasma concentrations and the frequency of P(+) cells, P(+) T cells, P(+) NK cells and their CD56(+dim) and CD56(+bright) subsets during the first week after the NSTEMI. The expression of P in NK cells was accompanied by P-mediated cytotoxicity against K-562 targets at all days examined, except day 21, when an anti-perforin monoclonal antibody did not completely abolish the killing. The percentage of P(+) T cells, P(+) NKT cells and P(+) NK subsets was the highest on the day 1 after NSTEMI and decreased in the post-infarction period. CD56(+) lymphocytes were found in damaged myocardium, suggesting their tissue recruitment. In conclusion, patients with NSTEMI have a strong and prolonged P-mediated systemic inflammatory reaction, which may sustain autoaggressive reactions towards myocardial tissue during the development of myocardial infarction.
authors.affiliation: Division of Cardiology, Hospital for Medical Rehabilitation of Hearth and Lung Diseases and Rheumatism Thalassotherapia-Opatija, Opatija, Croatia. Gordana.Laskarin@medri.hr
authors.forename: G
authors.initials: G
authors.lastname: Laskarin
authors.forename: V
authors.initials: V
authors.lastname: Persic
authors.forename: A
authors.initials: A
authors.lastname: Ruzic
authors.forename: B
authors.initials: B
authors.lastname: Miletic
authors.forename: M
authors.initials: M
authors.lastname: Rakic
authors.forename: D Travica
authors.initials: DT
authors.lastname: Samsa
authors.forename: D
authors.initials: D
authors.lastname: Raljevic
authors.forename: V Pehar
authors.initials: VP
authors.lastname: Pejcinovic
authors.forename: R
authors.initials: R
authors.lastname: Miskulin
authors.forename: D
authors.initials: D
authors.lastname: Rukavina
mesh_terms: D000368:Aged; D015551:Autoimmunity; D019002:CD56 Antigen / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D004562:Electrocardiography; D005260:Female; D006801:Humans; D020014:K562 Cells / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology; D055611:Natural Killer T-Cells / Q000276:immunology / Q000473:pathology; D054353:Perforin / Q000276:immunology*; D019210:Troponin I / Q000097:blood / Q000276:immunology
chemical_list: D019002:CD56 Antigen; C522918:NCAM1 protein, human; D019210:Troponin I; D054353:Perforin